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It’s not the size of a snake’s muscles that matter, but how it uses them. King snakes can defeat larger snakes in a wrestling match to the death because of how they coil around their prey, researchers report March 15 in the Journal of Experimental Biology.

King snakes wrap around their food and squeeze with about twice as much pressure as rat snakes do, says David Penning, a functional morphologist at Missouri Southern State University in Joplin. Penning, along with colleague Brad Moon at the University of Louisiana at Lafayette, measured the constriction capabilities of almost 200 snakes. “King snakes are just little brutes,” Penning says.
King snakes, which are common in North American forests and grasslands, are constrictor snakes that “wrestle for a living,” Penning says. They mainly eat rodents, birds and eggs, squeezing so hard, they can stop their prey’s heart (SN: 8/22/15, p. 4). In addition, about a quarter of the king snake diet is other snakes. King snakes can easily attack and eat vipers because they’re immune to the venom, but when they take on larger constrictors, such as rat snakes, it has been unclear what gives them the edge. “That’s not how nature goes,” Penning says, because predators are usually larger than their prey.

King snakes, though, can eat snakes up to 35 percent larger than themselves. One of the largest king snake conquests on record, from 1893, is of a 5-foot-3-inch rat snake, about 17 percent larger than the 4-foot-6-inch king snake that consumed it, Penning says.
“David Penning is really one of the first researchers that has been looking at the anatomy, physiology and function of these snakes” to understand how king snakes are superior to rat snakes, says Anthony Herrel, a functional morphologist and evolutionary biologist at the French National Museum of Natural History in Paris.
To determine what makes these snakes kings, Penning and Moon compared their muscle size, ability to escape attack and the strength of their squeeze to that of rat snakes. In one test, the researchers shook dead rodents enticingly in front of the snakes to goad them into striking and squeezing. Sensors on the rodents recorded the pressure of the squeeze.

The king snakes constricted with an average pressure of about 20 kilopascals, stronger than the pumping pressure of a human heart. Rat snakes in the same tests applied only about 10 kilopascals of pressure.

But the king snakes weren’t bigger body builders. Controlling for body size, the two kinds of snakes “had the exact same quantity of muscle,” Penning says.

The snakes’ more powerful constriction is probably due to how they use their muscles, not how much muscle they have, the researchers conclude. They observed that the majority of king snakes in the study wrapped around their food like a spring in what Penning calls the “curly fry pattern.” Rat snakes didn’t always coil in the same way and often ended up looking like a “weird pile of spaghetti,” he says.

Penning plans to study how other factors influence constriction as well, such as how long the king snakes can squeeze, how hungry they are and the temperature of their environment.

In the scientific version of her obituary, Dolly the Sheep was reported to have suffered from severe arthritis in her knees. The finding and Dolly’s early death from an infection led many researchers to think that cloning might cause animals to age prematurely.

But new X-rays of Dolly’s skeleton and those of other cloned sheep and Dolly’s naturally conceived daughter Bonnie indicate that the world’s first cloned mammal had the joints of normal sheep of her age. Just like other sheep, Dolly had a little bit of arthritis in her hips, knees and elbows, developmental biologist Kevin Sinclair of the University of Nottingham in England and colleagues report November 23 in Scientific Reports.
The researchers decided to reexamine Dolly’s remains after finding that her cloned “sisters” have aged normally and didn’t have massive arthritis (SN: 8/20/16, p. 6). No formal records of Dolly’s original arthritis exams were kept, so Sinclair and colleagues got Dolly’s and Bonnie’s skeletons and those of two other cloned sheep, Megan and Morag, from the National Museums Scotland in Edinburgh. Megan and Bonnie were both older than Dolly at the time of their deaths and had more bone damage than Dolly did. Morag died younger and had less damage.
Dolly’s arthritis levels were similar to those of naturally conceived sheep her age, indicating that cloning wasn’t to blame. “If there were a direct link with cloning and osteoarthritis, we would have expected to find a lot worse, and it would be more extensive and have a different distribution than what we’re finding in ordinary sheep,” says study coauthor Sandra Corr, a veterinary orthopedic specialist at the University of Glasgow in Scotland.
Dolly’s slightly creaky joints may have stemmed from giving birth to six lambs, including Bonnie. Pregnancy is a risk factor for arthritis in sheep.

For decades, the name “virus” meant small and simple. Not anymore. Meet the giants.

Today, scientists are finding ever bigger viruses that pack impressive amounts of genetic material. The era of the giant virus began in 2003 with the discovery of the first Mimivirus (SN: 5/23/09, p. 9). The viral titan is about 750 nanometers across with a genetic pantry boasting around 1.2 million base pairs of DNA, the information-toting bits often represented with A, T, C and G. Influenza A, for example, is roughly 100 nanometers across with only about 13,500 base pairs of genetic material.

In 2009, another giant virus called Marseillevirus was identified. It is different enough from mimiviruses to earn its own family. Since 2013, mega-sized viruses falling into another eight potential virus families have been found, showcasing a long-unexplored viral diversity, researchers reported last year in Annual Review of Virology and in January in Frontiers in Microbiology.

Giant viruses mostly come in two shapes: polyhedral capsules and egglike ovals. But one, Mollivirus, skews more spherical. Pacmanvirus was named for the broken appearance of its outer shell. Both represent potential families. Two newly discovered members of the mimivirus family, both called tupanviruses and both with tails, have the most complete set of genes related to assembling proteins yet seen in viruses (SN Online: 2/27/18). Once unheard of, giant viruses may be common in water and soils worldwide. Only time — and more discoveries — will tell.
Virus length and genome size for a representative from each of two recognized giant virus families (mimivirus and marseillevirus families) and eight potential families are shown. Circles are scaled to genome size and shaded by size range, with influenza A and E. coli bacterium included for comparison. Years indicate when the first viruses were described.

Graphic: C. Chang; Sources: P. Colson, B. La Scola and D. Raoult/Annual Review of Virology 2017; J. Andreani et al/Frontiers in Microbiology 2018

Perhaps the most unsettling scene in Poached, by science journalist Rachel Love Nuwer, comes early in the book, in a fancy restaurant in Ho Chi Minh City, Vietnam. The author and two friends sit down and are handed leather-bound menus offering roasted civet, fried tortoise, stewed pangolin and other delicacies made from rare or endangered species. The trio makes an abrupt exit, but only after seeing a live cobra gutted at one table and a still-living civet brought out to feed another group of diners.
Statistics on the illegal wildlife trade can be mind-numbing. Rhinos have dwindled to just 30,000 animals globally and tigers to fewer than 4,000. Over a million pangolins — scaly anteaters found in Africa and Asia — have been killed in the last 10 years. Just last month came a report from the Humane Society of the United States and the Humane Society International that the United States imported some 40,000 giraffe parts, from about 4,000 animals, between 2006 and 2015.

But in Poached, Nuwer gives readers a firsthand view of what the illegal wildlife trade is like on the ground and what, if anything, can be done to stop it. She accompanies a poacher into the U Minh forest of Vietnam in search of water monitors, cobras and civets. (Thankfully, they don’t find any.) She has dinner with a man who keeps a rhino horn in an Oreo tin. She visits a zoo in Japan that may have helped popularize trade in the rare earless monitor lizard. And she attends numerous meetings of wildlife officials and conservationists as they attempt to fight back against the illegal trade.

Poached isn’t all gloom and doom; there are a few success stories. Nuwer, for instance, visits Zakouma National Park in Chad where managers have halted the slaughter of elephants. This hard-won accomplishment exemplifies the book’s underlying message: There are no easy solutions to stopping wildlife trafficking. The effort in Zakouma required a lot of money and training for its rangers, which is not available in most places.

What’s most needed, Nuwer argues, is changing how we think about wildlife crime. Many people view poaching as belonging to a special category of illegal activity. But it’s not; it’s just crime. Those involved are often also dealing in drugs or conflict diamonds or human trafficking. A change in mind-set could help overcome a major conservation obstacle, Nuwer notes. Rather than detectives and the courts being tasked with handling this sort of crime, the job has been left to rangers, wildlife managers and conservationists. “As some have put it,” she writes, “it is like asking botanists to stop the cocaine trade.” The world’s wildlife deserves better than that.

Mayflies swarming a central Pennsylvania bridge over the Susquehanna River are a good thing, and a bad thing. Before the 1972 Clean Water Act, the river was too polluted to support the primitive aquatic insects. So their comeback is a sign that the water is healthier, says forensic entomologist John Wallace of nearby Millersville University.

But those swarms have become a nighttime menace for people driving or walking across the Columbia-Wrightsville bridge — thanks to the 2014 installation of large, 1930-era lamps along the two sides of the bridge. Soon after the lights were added, adult mayflies of the species Hexaginia bilineata began invading — causing blizzard-like conditions on the 2-kilometer overpass. The swarms were so intense in 2015, the bridge was closed following three accidents, and bulldozers were brought in to remove knee-deep piles of insect carcasses.
Local officials have since tried to cope by occasionally turning off the lights, but this is problematic on a high-traffic bridge, says Wrightsville borough president Eric White. So Wallace was called in this year to make sense of the mayfly madness.

Wallace says he and undergraduate student Marisa Macchia have been collecting specimens from both sides of the bridge, and “comparing the mayfly abundance and diversity when lights are on versus when lights [are] off.” The researchers are trying to determine the swarm density per hour from the start of the emergence to the end.
As larvae, mayflies drift downstream with the water current, Wallace says. When the adults emerge from the water, they fly upriver, following the water’s moonlit path of polarized light. At the end of their adult life spans of 24-48 hours, the insects mate and the females drop to the water’s surface — dying while releasing their eggs to the silt below.
But that bridge, with those lamps, is breaking that path of polarized light, luring the mayflies up to the structure and causing the confused insects to perform their “drop, deposit and die” routine on the road.

“Any human light … car light, street light — are examples of unpolarized light,” Wallace says. But when reflected off asphalt or car paint, it resembles the river’s polarized light.

Wallace’s research will inform blueprints for renovating the historic bridge, White says. The goal is ultimately to guide the mayflies back to the river’s surface.

When you’re stressed and anxious, you might feel your heart race. Is your heart racing because you’re afraid? Or does your speeding heart itself contribute to your anxiety? Both could be true, a new study in mice suggests.

By artificially increasing the heart rates of mice, scientists were able to increase anxiety-like behaviors — ones that the team then calmed by turning off a particular part of the brain. The study, published in the March 9 Nature, shows that in high-risk contexts, a racing heart could go to your head and increase anxiety. The findings could offer a new angle for studying and, potentially, treating anxiety disorders.
The idea that body sensations might contribute to emotions in the brain goes back at least to one of the founders of psychology, William James, says Karl Deisseroth, a neuroscientist at Stanford University. In James’ 1890 book The Principles of Psychology, he put forward the idea that emotion follows what the body experiences. “We feel sorry because we cry, angry because we strike, afraid because we tremble,” James wrote.

The brain certainly can sense internal body signals, a phenomenon called interoception. But whether those sensations — like a racing heart — can contribute to emotion is difficult to prove, says Anna Beyeler, a neuroscientist at the French National Institute of Health and Medical Research in Bordeaux. She studies brain circuitry related to emotion and wrote a commentary on the new study but was not involved in the research. “I’m sure a lot of people have thought of doing these experiments, but no one really had the tools,” she says.

Deisseroth has spent his career developing those tools. He is one of the scientists who developed optogenetics — a technique that uses viruses to modify the genes of specific cells to respond to bursts of light (SN: 6/18/21; SN: 1/15/10). Scientists can use the flip of a light switch to activate or suppress the activity of those cells.
In the new study, Deisseroth and his colleagues used a light attached to a tiny vest over a mouse’s genetically engineered heart to change the animal’s heart rate. When the light was off, a mouse’s heart pumped at about 600 beats per minute. But when the team turned on a light that flashed at 900 beats per minutes, the mouse’s heartbeat followed suit. “It’s a nice reasonable acceleration, [one a mouse] would encounter in a time of stress or fear,” Deisseroth explains.

When the mice felt their hearts racing, they showed anxiety-like behavior. In risky scenarios — like open areas where a little mouse might be someone’s lunch — the rodents slunk along the walls and lurked in darker corners. When pressing a lever for water that could sometimes be coupled with a mild shock, mice with normal heart rates still pressed without hesitation. But mice with racing hearts decided they’d rather go thirsty.

“Everybody was expecting that, but it’s the first time that it has been clearly demonstrated,” Beyeler says.
The researchers also scanned the animals’ brains to find areas that might be processing the increased heart rate. One of the biggest signals, Deisseroth says, came from the posterior insula (SN: 4/25/16). “The insula was interesting because it’s highly connected with interoceptive circuitry,” he explains. “When we saw that signal, [our] interest was definitely piqued.”

Using more optogenetics, the team reduced activity in the posterior insula, which decreased the mice’s anxiety-like behaviors. The animals’ hearts still raced, but they behaved more normally, spending some time in open areas of mazes and pressing levers for water without fear.
A lot of people are very excited about the work, says Wen Chen, the branch chief of basic medicine research for complementary and integrative health at the National Center for Complementary and Integrative Health in Bethesda, Md. “No matter what kind of meetings I go into, in the last two days, everybody brought up this paper,” says Chen, who wasn’t involved in the research.

The next step, Deisseroth says, is to look at other parts of the body that might affect anxiety. “We can feel it in our gut sometimes, or we can feel it in our neck or shoulders,” he says. Using optogenetics to tense a mouse’s muscles, or give them tummy butterflies, might reveal other pathways that produce fearful or anxiety-like behaviors.

Understanding the link between heart and head could eventually factor into how doctors treat panic and anxiety, Beyeler says. But the path between the lab and the clinic, she notes, is much more convoluted than that of the heart to the head.

An experimental treatment for endometriosis, a painful gynecological disease that affects some 190 million people worldwide, may one day offer new hope for easing symptoms.

Monthly antibody injections reversed telltale signs of endometriosis in monkeys, researchers report February 22 in Science Translational Medicine. The antibody targets IL-8, a molecule that whips up inflammation inside the scattered, sometimes bleeding lesions that mark the disease. After neutralizing IL-8, those hallmark lesions shrink, the team found.

The new treatment is “pretty potent,” says Philippa Saunders, a reproductive scientist at the University of Edinburgh who was not involved with work. The study’s authors haven’t reported a cure, she points out, but their antibody does seem to have an impact. “I think it’s really very promising,” she says.

Many scientists think endometriosis occurs when bits of the uterine lining — the endometrium — slough off during menstruation. Instead of exiting via the vagina, they voyage in the other direction: up through the fallopian tubes. Those bits of tissue then trespass through the body, sprouting lesions where they land. They’ll glom onto the ovaries, fallopian tubes, bladder and other spots outside of the uterus and take on a life of their own, Saunders says.
The lesions can grow nerve cells, form tough nubs of tissue and even bleed during menstrual cycles. They can also kick off chronic bouts of pelvic pain. If you have endometriosis, you can experience “pain when you urinate, pain when you defecate, pain when you have sex, pain when you move around,” Saunders says. People with the disease can also struggle with infertility and depression, she adds. “It’s really nasty.”
Once diagnosed, patients face a dearth of treatment options — there’s no cure, only therapies to alleviate symptoms. Surgery to remove lesions can help, but symptoms often come back.

The disease affects at least 10 percent of girls, women and transgender men in their reproductive years, Saunders says. And people typically suffer for years — about eight on average — before a diagnosis. “Doctors consider menstrual pelvic pain a very common thing,” says Ayako Nishimoto-Kakiuchi, a pharmacologist at Chugai Pharmaceutical Co. Ltd. in Tokyo. Endometriosis “is underestimated in the clinic,” she says. “I strongly believe that this disease has been understudied.”

Hormonal drugs that stop ovulation and menstruation can also offer relief, says Serdar Bulun, a reproductive endocrinologist at Northwestern University Feinberg School of Medicine in Chicago not involved with the new study. But those drugs come with side effects and aren’t ideal for people trying to become pregnant. “I see these patients day in and day out,” he says. “I see how much they suffer, and I feel like we are not doing enough.”

Nishimoto-Kakiuchi’s team engineered an antibody that grabs onto the inflammatory factor IL-8, a protein that scientists have previously fingered as one potential culprit in the disease. The antibody acts like a garbage collector, Nishimoto-Kakiuchi says. It grabs IL-8, delivers it to the cell’s waste disposal machinery, and then heads out to snare more IL-8.

The team tested the antibody in cynomolgus monkeys that were surgically modified to have the disease. (Endometriosis rarely shows up spontaneously in these monkeys, the scientists discovered previously after screening more than 600 females.) The team treated 11 monkeys with the antibody injection once a month for six months. In these animals, lesions shriveled and the adhesive tissue that glues them to the body thinned out, too. Before this study, Nishimoto-Kakiuchi says, the team didn’t think such signs of endometriosis were reversible.
Her company has now started a Phase I clinical trial to test the safety of therapy in humans. The treatment is one of several endometriosis therapies scientists are testing (SN: 7/19/19) . Other trials will test new hormonal drugs, robot-assisted surgery and behavioral interventions.

Doctors need new options to help people with the disease, Saunders says. “There’s a huge unmet clinical need.”

SpaceX’s rapidly growing fleet of Starlink internet satellites now make up half of all active satellites in Earth orbit.

On February 27, the aerospace company launched 21 new satellites to join its broadband internet Starlink fleet. That brought the total number of active Starlink satellites to 3,660, or about 50 percent of the nearly 7,300 active satellites in orbit, according to analysis by astronomer Jonathan McDowell using data from SpaceX and the U.S. Space Force.
“These big low-orbit internet constellations have come from nowhere in 2019, to dominating the space environment in 2023,” says McDowell, of the Harvard-Smithsonian Center for Astrophysics in Cambridge, Mass. “It really is a massive shift and a massive industrialization of low orbit.”

SpaceX has been launching Starlink satellites since 2019 with the goal of bringing broadband internet to remote parts of the globe. And for just as long, astronomers have been warning that the bright satellites could mess up their view of the cosmos by leaving streaks on telescope images as they glide past (SN: 3/12/20).

Even the Hubble Space Telescope, which orbits more than 500 kilometers above the Earth’s surface, is vulnerable to these satellite streaks, as well as those from other satellite constellations. From 2002 to 2021, the percentage of Hubble images affected by light from low-orbit satellites increased by about 50 percent, astronomer Sandor Kruk of the Max-Planck Institute for Extraterrestrial Physics in Garching, Germany, and colleagues report March 2 in Nature Astronomy.

The number of images partially blocked by satellites is still small, the team found, rising from nearly 3 percent of images taken between 2002 and 2005 to just over 4 percent between 2018 and 2021 for one of Hubble’s cameras. But there are already thousands more Starlink satellites now than there were in 2021.

“The fraction of [Hubble] images crossed by satellites is currently small with a negligible impact on science,” Kruk and colleagues write. “However, the number of satellites and space debris will only increase in the future.” The team predicts that by the 2030s, the probability of a satellite crossing Hubble’s field of view any time it takes an image will be between 20 and 50 percent.
The sudden jump in Starlink satellites also poses a problem for space traffic, says astronomer Samantha Lawler of the University of Regina in Canada. Starlink satellites all orbit at a similar distance from Earth, just above 500 kilometers.

“Starlink is the densest patch of space that has ever existed,” Lawler says. The satellites are constantly navigating out of each other’s way to avoid collisions (SN: 2/12/09). And it’s a popular orbital altitude — Hubble is there, and so is the International Space Station and the Chinese space station.
“If there is some kind of collision [between Starlinks], some kind of mishap, it could immediately affect human lives,” Lawler says.

SpaceX launches Starlink satellites roughly once per week — it launched 51 more on March 3. And they’re not the only company launching constellations of internet satellites. By the 2030s, there could be 100,000 satellites crowding low Earth orbit.

So far, there are no international regulations to curb the number of satellites a private company can launch or to limit which orbits they can occupy.

“The speed of commercial development is much faster than the speed of regulation change,” McDowell says. “There needs to be an overhaul of space traffic management and space regulation generally to cope with these massive commercial projects.”

The oldest known fossils of pollen-laden insects are of earwig-like ground-dwellers that lived in what is now Russia about 280 million years ago, researchers report. Their finding pushes back the fossil record of insects transporting pollen from one plant to another, a key aspect of modern-day pollination, by about 120 million years.

The insects — from a pollen-eating genus named Tillyardembia first described in 1937 — were typically about 1.5 centimeters long, says Alexander Khramov, a paleoentomologist at the Borissiak Paleontological Institute in Moscow. Flimsy wings probably kept the creatures mostly on the forest floor, he says, leaving them to climb trees to find and consume their pollen.

Recently, Khramov and his colleagues scrutinized 425 fossils of Tillyardembia in the institute’s collection. Six had clumps of pollen grains trapped on their heads, legs, thoraxes or abdomens, the team reports February 28 in Biology Letters. A proportion that small isn’t surprising, Khramov says, because the fossils were preserved in what started out as fine-grained sediments. The early stages of fossilization in such material would tend to wash away pollen from the insects’ remains.
The pollen-laden insects had only a couple of types of pollen trapped on them, the team found, suggesting that the critters were very selective in the tree species they visited. “That sort of specialization is in line with potential pollinators,” says Michael Engel, a paleoentomologist at the University of Kansas in Lawrence who was not involved in the study. “There’s probably vast amounts of such specialization that occurred even before Tillyardembia, we just don’t have evidence of it yet.”

Further study of these fossils might reveal if Tillyardembia had evolved special pollen-trapping hairs or other such structures on their bodies or heads, says Conrad Labandeira, a paleoecologist at the National Museum of Natural History in Washington, D.C., also not part of the study. It would also be interesting, he says, to see if something about the pollen helped it stick to the insects. If the pollen grains had structures that enabled them to clump more readily, for example, then those same features may have helped them grab Velcro-like onto any hairlike structures on the insects’ bodies.

Fungi may help some tree-killer beetles turn a tree’s natural defense system against itself.

The Eurasian spruce bark beetle (Ips typographus) has massacred millions of conifers in forests across Europe. Now, research suggests that fungi associated with these bark beetles are key players in the insect’s hostile takeovers. These fungi warp the chemical defenses of host trees to create an aroma that attracts beetles to burrow, researchers report February 21 in PLOS Biology.

This fungi-made perfume might explain why bark beetles tend to swarm the same tree. As climate change makes Europe’s forests more vulnerable to insect invasions, understanding this relationship could help scientists develop new countermeasures to ward off beetle attacks.
Bark beetles are a type of insect found around the world that feed and breed inside trees (SN: 12/17/10). In recent years, several bark beetle species have aggressively attacked forests from North America to Australia, leaving ominous strands of dead trees in their wake.

But trees aren’t defenseless. Conifers — which include pine and fir trees — are veritable chemical weapons factories. The evergreen smell of Christmas trees and alpine forests comes from airborne varieties of these chemicals. But while they may smell delightful, these chemicals’ main purpose is to trap and poison invaders.

Or at least, that’s what they’re meant to do.

“Conifers are full of resin and other stuff that should do horrible things to insects,” says Jonathan Gershenzon, a chemical ecologist at the Max Planck Institute for Chemical Ecology in Jena, Germany. “But bark beetles don’t seem to mind at all.”

This ability of bark beetles to overcome the powerful defense system of conifers has led some scientists to wonder if fungi might be helping. Fungi break down compounds in their environment for food and protection (SN: 11/30/21). And some type of fungi — including some species in the genus Grosmannia — are always found in association with Eurasian spruce bark beetles.
Gershenzon and his colleagues compared the chemicals released by spruce bark infested with Grosmannia and other fungi to the chemical profile of uninfected trees. The presence of the fungi fundamentally changed the chemical profile of spruce trees, the team found. More than half the airborne chemicals — made by fungi breaking down monoterpenes and other chemicals that are likely part of the tree defense system — were unique to infected trees after 12 days.

This is surprising because researchers had previously assumed that invading fungi hardly changed the chemical profile of trees, says Jonathan Cale, a fungal ecologist at the University of Northern British Columbia in Prince George, Canada, who was not involved with the research.
Later experiments revealed that bark beetles can detect many of these fungi-made chemicals. The team tested this by attaching tiny electrodes on bark beetles’ heads and detecting electrical activity when the chemicals wafted passed their antennae. What’s more, the smell of these chemicals combined with beetle pheromones led the insects to burrow at higher rates than the smell of pheromones alone.

The study suggests that these fungi-made chemicals can help beetles tell where to feed and breed, possibly by advertising that the fungi has taken down some of the tree’s defenses. The attractive nature of the chemicals could also explain the beetle’s swarming behavior, which drives the death of healthy adult trees.

But while the fungi aroma might doom trees, it could also lead to the beetles’ demise. Beetle traps in Europe currently use only beetle pheromones to attract their victims. Combining pheromones with fungi-derived chemicals might be the secret to entice more beetles into traps, making them more effective.

The results present “an exciting direction for developing new tools to manage destructive bark beetle outbreaks” for other beetle species as well, Cale says. In North America, mild winters and drought have put conifer forests at greater risk from mountain pine beetle (Dendroctonus pendersoae) attacks. Finding and using fungi-derived chemicals might be one way to fend off the worst of the bark beetle invasions in years to come.